Mean arterial pressure model

Witte, D.G. Brune, M.E. Katwala, S.P. Milicic, I. Stolarik, D. Hui, Y.-H. Marsh, K.C. Kerwin, J.F., Jr. Meyer, M.D. Hancock, A.A. Modeling of relationships between pharmacokinetics and blockade of agonist-indued elevation of intraurethral pressure and mean arterial pressure in conscious dogs treated with al-adrenoceptro antagonists. J. Pharmacol. Exp. Ther. 2002, 300 (2), 495-504. 

The role of ventricular resistance in the coupling of the ventricle to its arterial load was also investigated. For this purpose, a computer simulation study was performed where the LV was represented by the above model and the arterial load by a modified Windkessel (i.e., peripheral resistance, lumped arterial compliance and a characteristic impedance). It was observed that inclusion of a ventricular resistance slightly decreased mean arterial pressure (3 to 10%) and stroke volume (3 to 7%). In contrast, the pulsatile nature of the flow was markedly altered suggesting that ventricular resistance may play an important role in minimizing the external pulsatile power and in optimally coupling the ventricle to its arterial load (Shroff et ai, 1983a). 

Following the infusion into mammals of most, if not all, tHb solutions, increases in mean arterial and pulmonary artery pressures and systemic and pulmonary vascular resistances are observed. The observations vary with the species and the preclinical or clinical model being studied. For the most part, the increases in MAP are rapid but apparently self-limiting (i.e., there is no continuous, dose-related escalation). Their duration apparently depends on the structure or some other property of the Hb infusate and the dose administered. 

There has been very little work to date on first-generation models of neural n-3 deficiency. Weisinger et al. found effects of postnatal n-3 deprivation on electroretinographic responses in guinea pigs (28) and mean arterial blood pressure in rats (29). Ward et al. (30) showed that gastrostomy feeding of safflower oil-based diet to rats from d 5 of life to adulthood led to an 50% decline in brain DHA. Connor et al. (31) observed a marked decrease in brain and retinal DHA in rhesus monkeys that had been fed a safflower oil-based diet from birth. 

Figure 3. The arterial pressure (P ) and central venous pressure (F ) as functions of the systemic flow (Q) in the model depicted in Figure 1, where R = 20 and C,7C = 19. Point a denotes the value of the mean systemic pressure i e., the common value for and/ ,. when Q = 0. Points b and c denote the values of P and P, when 0 == 1, and points d and e, the values of P and P, when 0 = 5. The deviations of P and P, from P , are denoted by zlP andJP,., respectively. Note that the scales for P and Py are not the same. (From Levy, with permission of the American Heart Assoc., Inc.)...

Spontaneously hypertensive rats can be used to screen compounds for antihypertensive effects and for effects on heart rate. The animals are dosed for one or a few days. Blood pressure and heart rate are measured by means of an inflatable cuff around the tail. Most classes of antihypertensives will be detected. Agents such as beta-adrenergic antagonists will be detected by decreased heart rate. Other rat models include deoxycorticosterone acetate (DOCA)-induced hypertensive, renal hypertensive (one or both renal arteries clamped), and stroke-prone spontaneously hypertensive rats. Hypertensive dogs produced by clamping one or both renal arteries may also be used to test or verify antihypertensive activity in a second species. 

Baroreceptors monitor the pressure in the carotid sinuses, the aortic arch, and other large systemic arteries and increase their firing rate when the pressure increases. Their response is nonlinear and depends on whether they are exposed to mean pressure only, pulsatile pressure only, or a combination of both. Katona et al. [1967] developed a model of baroreceptor feedback that has become the basis for many CV neural control models. The output of the baroreceptor model is often passed through a low pass filter representing the CNS and then mapped back to changes in heart rate, contractility, vascular resistances, and vascular unstressed volumes through the sympathetic and parasympathetic nervous systems (Figure 10.8), for example, see Yu et al. [1990]. 

There has not been any prior analytical investigation of the arterial stiffening theory of pseudohypertension. The low arterial comphance theory is tested in this chapter via a mathematical model of oscillometric blood pressure measurement. The computational model will be used to evaluate measurement error introduced by arterial disease or alterations in arterial mechanics in general. Once these errors are established, the model will then be used to investigate the means by which automated blood pressure monitor may detect the occurrence of pseudo-hypertension or provide a correction method by which blood pressure accuracy is unproved even in the presence of arterial disease. 

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